By Emma Young
The head of a brown lion. Multiple tiny, green, spinning Catherine wheels with red edges. Colourful fragments of artillery soldiers and figures in uniform and action. Unfamiliar faces of well-groomed men… These are just a few of the hallucinations reported by a group of people with macular degeneration (MD), a common cause of vision loss in people aged over 40.
About 40 per cent of people with MD – who lose vision in the centre of their visual field but whose peripheral vision is generally unaffected – develop Charles Bonnet syndrome (CBS), reporting hallucinations that vary from simple flashes of light and shapes to faces, animals and even complex scenes.
It has been suggested that CBS might arise as a result of over-responsiveness – “hyper-excitability” – of certain visual regions of the cortex, after they are deprived of normal retinal input. But whether this really is the case – and why some people with reduced vision or blindness develop them, while others don’t – has not been clear. Now new work by a team of psychologists at the University of Queensland, Australia, led by David Painter, and published in Current Biology, offers some answers.
Painter and his team studied eight people with MD and Charles Bonnet syndrome (whose regular hallucinations include those listed at the start of this post); eight age- and gender-matched people with MD but without CBS; and eight matched controls with healthy eyes.
The researchers presented the participants with a series of red and green flickering chequerboard patterns, to stimulate the intact peripheral region of their retinas. Using EEG (electroencephalography) to monitor the participants’ brain activity, the researchers found a much bigger response to the flickering patterns in the early vision processing regions of the cortex in the people with MD who also have CBS, compared with both the other groups.
None of the CBS participants reported experiencing hallucinations during the study, so hyper-excitability of these visual processing regions does not automatically trigger hallucinations, but does seem to be a feature of the brains of people who are susceptible to them.
The precise triggers for hallucinations in people with CBS vary. They include low light levels, or watching TV or riding in a car. Exactly how these triggers might interact with the over-responsiveness of the visual cortex to generate hallucinations is yet to be explored.
Unlike people with schizophrenia, individuals with CBS usually have no trouble recognising that their hallucinations are not real, and most don’t find them distressing. However a minority do, and further research may lead to treatments, write Painter and his colleagues.
“Based on our findings, future treatments could aim to down-regulate cortical hyperexcitability in CBS,” they write, “perhaps through repeated application of non-invasive brain stimulation protocols that induce long-lasting plastic changes in underlying cortical networks.”
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